Human studies suggest that maternal viral infection during pregnancy correlates with an increased frequency of Autism Spectrum Disorder (ASD) in the offspring (1-6). This observation has been modeled in rodents subjected to maternal immune activation (MIA) (7). The immune cell populations involved in induction of ASD-like behavior in the MIA model have not, however, been identified. A number of inflammatory cytokines and chemokines have been implicated in MIA, including tumor necrosis factor-α (TNF-α), IL-1β, and IL-8. Accordingly, information available to date demonstrates that a variety of inflammatory molecules contribute to MIA and thus, MIA is viewed as a generalized state of inflammation. See, for example, Harvey et al. (2014, Brain Behav Immun 40:27), Washington et al. (2015, Epilepsy Behav 50:40), and Ballendine et al. (2015, Prog Neuropsychopharmacol Biol Psychiatry 57:155), the entire content of each of which is incorporated herein by reference. The mechanism/s whereby inflammatory cytokines and chemokines contribute to MIA and MIA contributes to the development of autism and the specific immune cell population(s) involved are unknown.
The citation of references herein shall not be construed as an admission that such is prior art to the present invention.